The murine B-cell tumor, BCL1, expresses both IgM and IgD on its surface and is inducible by mitogens to secrete greater levels of IgM in vitro. A nonsecreting subclone of the tumor has been developed which responds to BCDF mu, a lymphokine present in PK7.1 T-cell supernatants, by increasing its transcription of mu's mRNA and concomitant secretion of IgM. This subclone is currently being investigated as a target cell for BCDF gamma, another lymphokine present in PK7.1 supernatants. Conditions have been established for this factor with purified splenic B\cells for specific induction of IgG1 message and protein while IgG2b and IgG3 synthesis is suppressed. Several putative switch variants of the BCL1 line have been isolated and are under molecular characterization. The principal goal is to establish the precise mechanism and point of recombination for a T-dependent isotype switch.